Low atmospheric pressure stunning (LAPS) is a novel approach to pre-slaughter stunning of chickens using progressive hypobaric hypoxia by the application of gradual decompression (280s cycle) according to a set of prescribed pressure curves. Low atmospheric pressure stunning produces a non-recovery state. Concerns have been raised relating to the possible pathological and welfare consequences of expansion of air in the body during LAPS. In a randomised trial, we compared the gross pathology of broilers exposed to LAPS with a control group euthanised by intravenous injection of pentobarbital sodium (60 mixed sex broilers per treatment). The birds were exposed to each treatment in triplets and all birds were subject to necropsy examination to detect and score (1 to 5, minimal to severe) haemorrhagic lesions or congestion for all major organs and cavities (e.g. air sacs, joints, ears and heart) as well as external assessment for product quality (e.g. wing tips). Behavioural data (latency to loss of posture and motionless) and chamber cycle data (temperature, humidity, pressure and oxygen availability) confirmed that LAPS had been applied in a manner representative of the commercial process. All of the organs observed were structurally intact for both treatment groups. No lesions were observed in the external ears, oral cavity, tracheal lumen, crop and air sacs of birds from either treatment group. There was no difference between treatments in the wingtips, nasal turbinates, thymus, biceps femoralis and colon. Haemorrhagic lesions were observed in the calvaria, brains, hearts and lungs of both treatment groups, but lesions in these areas were more severe in the LAPS treatment group. It was not possible to distinguish between pathological changes induced by decompression or recompression. In the barbiturate group, more severe haemorrhagic lesions were observed in the superficial pectoral muscles as well as greater congestion of the infraorbital sinuses, liver, spleens, duodenum, kidneys and gonads. These findings provide evidence that LAPS did not result in distension of the intestines and air sacs sufficient to cause changes, which were grossly visible on postmortem examination. There was also no evidence of barotrauma in the ears and sinuses. The pathological changes observed in the barbiturate treatment were as expected based on barbiturate toxicity. Low atmospheric pressure stunning appears to produce pathological changes by a variety of well-established mechanisms, and while these pathological data have limited value as welfare indicators, the results confirm that organ integrity was not compromised by the process.

Effects of extreme environments on food intake in human subjects are analysed as behavioural and physiological adaptations to annual and circadian rhythms, temperature and altitude. Effects of the environment on food intake through food availability have direct consequences on energy balance and body weight. Different geographical regions show variations in the composition of dietary foods, i.e. the relative proportions of carbohydrate, protein and fat. In developing countries the annual cycle appears to affect body weight through dependence on food availability. In West-European countries this effect appears to depend on physical activity. Energy and macronutrient intakes appear to follow a circadian pattern, with breakfast being relatively high in carbohydrate and dinner being relatively high in fat. In cold conditions, maintaining an adequate food intake is important in sustaining normal physiological responses to cold. Evidence for a possible cold-induced increase in appetite is poor. A condition influencing level of intake is the palatability of the food. High altitude, i.e. hypobaric hypoxia, appears to reduce appetite, energy intake and body mass, irrespective of acute mountain sickness (AMS). Meal size is reduced and meal frequency increased. Under circumstances of AMS, dissociation between appetite and hunger occurs. Thus, spontaneous adaptation to extreme environments requiring increased energy intake occurs first by adaptation of body weight to a new energy balance. In general, prevention of a negative energy balance occurs by learning with respect to food intake. After return to normal, adjustment of energy intake to the original energy balance occurs with restoration of body weight.